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She was slow and unable to complete tasks and left school prematurely because of the pressure to complete assignments and the disgrace of poor achievement cheap rogaine 2 60 ml amex. She did not want responsible jobs because they were more difficult for her to complete generic 60 ml rogaine 2 with amex. She was an intelligent individual with a good understanding of her problems buy rogaine 2 60 ml cheap, but she felt powerless to conduct her life in the manner she wished purchase rogaine 2 60 ml mastercard. She was unduly concerned about her bed covers having creases, and could not leave her room until she was convinced there were none. She was distressed by the letter “R” because it suggested “rape”. When she saw the letter “R” on a signpost or advertisement she have the compulsion of saying various words to herself, starting with the word “rape” and then moving off to totally unrelated words, i. Ms D did not have a particular fear of being raped herself, it was simply that the word made her intensely uncomfortable. There was an examination couch with a covering sheet in the office. Folds and wrinkles were made in the sheet by the psychiatrist at the start of each interview, she was asked not to remove them. She was then distracted by the psychiatrist during supportive psychotherapy and discussions about medication were conducted. She was able to tolerate this exposure and commenced resisting her compulsion at home. The compulsion to repeat words after seeing the letter R was treated with thought stopping. She was shown the letter R and instructed to shout STOP and then switch her attention directly back to the task at hand. Within one week she was able to forcefully say STOP to herself, and switch to a productive task. Ms D was commenced on escitalopram which was gradually increased to 60 mg daily. She was placed in a work rehabilitation program, and was found suitable receptionist office work. She was able to leave her bed unmade and largely ignore the letter R. Ms D was seen for a few sessions on two subsequent occasions in the following two years, when stressful events appeared to have triggered minor set-backs. Case history, 2 Mr E was 55 years of age at the time of presentation. He was unemployed and lived in a small house with a railway track at the back. He had been known to the psychiatrist 25 years earlier when he was profoundly hypochondriacal and supported by his wife in his (mistaken) belief that he had various medical complaints which needed medical treatment. At presentation Mr E was very unclean and odoriferous. His hands were dirty and his nicotine stained nails were over 1 cm long and curling over the ends of his fingers. He stated that his medication was not correct because he developed light-headedness at 10:23 every morning. When asked about his neglected personal hygiene he did not address the question, but began talking about the need for cleanliness and about the health dangers of toilets. He was soon talking about his various hypochondriacal concerns. Mrs E explained that the patient was concerned about the cleanliness of all toilets, including that in his own home. Rather than risk getting germs from his toilet he had been in the habit, for some years, of opening his bowels at the side of the railway track behind his house. Public officials had become aware of this practice and had, on a number of occasions, threatened to prosecute. Mr E had again been threatened with prosecution in the week before admission, which may have caused a worsening in his mental state. Mrs E also stated that she was feeling overwhelmed by looking after her husband and doubted she would be able to remain with him. He was already taking a sufficient dose of and SSRI. A small dose of an atypical antipsychotic was added. He could not co-operate with behavioural therapy designed for his particular obsessions and compulsions. However, he was asked to use the toilet and interact with staff and other patients in Pridmore S. Over some weeks, however, his condition improved and he was able to use the toilet. Mrs E benefited from the rest and was happy to continue to support her husband at home. This case illustrates the paradox of some OCD patients who are concerned about cleanliness, but who are themselves, quite unclean. It seems that their concerns and the anxiety are so great and preoccupying that they are unaware of the facts of their actual situation. Case history, 3 Mr F was a 54-year-old divorced, unemployed former clerk, living alone in a Housing Department unit. His marriage had ended 20 years previously and he one child, a daughter living in a distant part of the country. He stated that he would not have been able to come alone because leaving his home was anxiety provoking. He had two friends from the distant past and had maintained contact with them by telephone. He reported that there had been a problem with his kitchen tap and he had not been able to turn it on for 7 years. Mr F could afford a plumber, but the stress of having another person in his flat was too much to contemplate. He had tried a vast range of medications over the years. He said that none had helped in the slightest and he had experienced severe side effects with most of them. His reluctance to leave the house appeared to be agoraphobia. He was disabled by an obsession that he may lose letters from his letter-box.

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Manual searching 182 15 Information needs of medical records from 1 practice (N=492 with stages 3–5 CKD identified by computer searching) was used to test the validity of computer searching to estimate the prevalence of CKD buy rogaine 2 60 ml visa. Serum creatinine measurements were calibrated to the original MDRD study in Stevens et al cheap rogaine 2 60 ml online. Two publications from the Optimal Renal Care UK (ORC UK) study assessed the utility of a disease management programme (DMP) that was guideline- and algorithm-based to identify order rogaine 2 60 ml online, manage safe rogaine 2 60 ml, and appropriately refer people with CKD. Medications dispensed prior to the index creatinine measurements were used to determine disease categories, which were considered in a stepwise logistic regression analysis. Risk scores were calculated for each subject and then categorised into risk classes (I to V). Another study investigated the ability of the Framingham prediction equation to predict 5 year and 10 year risk of cardiac events (myocardial infarction and fatal coronary heart disease) in people with CKD from the pooled ARIC and CHS studies (N=934). Manual checking of medical records identified only 4 additional cases of CKD missed by the computer search. The recording of a renal diagnosis improved as renal function declined. Only 270/1313 (20%) of people with diabetes, hypertension, and eGFR <60 ml/min/1. In people with stage 3–5 CKD without diabetes and a PCR <100, the percentage of systolic blood pressure measurements in target range increased significantly after 9 months of the DMP (37. In people with stage 3–5 CKD, with diabetes or a PCR >100, there were NS differences in blood pressure measurements in target range at baseline compared to after 9 months on the DMP. This was also true for people with eGFR fall ≥5 ml/min/1. After introduction of a referral assessment service, the referral rate decreased rapidly and by 6 months, an average of five new CKD stage 4 or 5 patients were being referred (0. This referral rate was within the capacity of local nephrology services. In both the derivation (N=6789) and validation cohorts (N=3395), people in the Class V risk index had triple the risk of rapid renal disease progression compared with people in the Class I risk index. The Framingham equation correctly identified men with CKD who would develop a cardiac event within 10 years only 184 15 Information needs 60% of the time, compared with 69% of the time in the non-CKD male cohort and 73% in the original Framingham cohort. In women with CKD, discrimination was 73% for 10-year cardiac events compared with 76% in the original Framingham cohort. The 5-year calibration for men was poor (chi-square 33. The Framingham equation under-predicted cardiac events in women with CKD and had poor 5- and 10-year calibration. Recalibrated models performed better, although prediction remained poor in men with CKD. In women with CKD, re-calibration showed NS difference in predicted and observed cardiac events in 5- and 10-year probability models. It was also prior to the introduction of appropriate Read Codes and the renal NSF. All of these factors may have subsequently improved the identification of CKD in primary care populations. Nevertheless the GDG agreed that it was still possible that people with an abnormal GFR or proteinuria were not classified as having CKD. As this information is usually recorded on practice computer databases it appears that it would be quite simple to devise programmes to identify these people. The introduction of a disease management programme tailored to people with CKD resulted in significant improvements in blood pressure and lipid control. A significant reduction in progression of CKD also followed the introduction of the disease management programme. The GDG were surprised that the tool for predicting rapid decline in kidney function did not include known factors such as hypertension and proteinuria in the score whilst anti-emetic use was. It was agreed that the anti-emetic use was probably a marker of the presence of an acute illness which may have affected GFR. The GDG agreed that separate tools for the identification of people with CKD and the identification of people with CKD at risk of progressing would be useful. UK: London: National Institute for Health and Clinical Excellence, 2007. National Service Framework for Renal Services – Part Two: Chronic kidney disease, acute renal failure and end of life care. Prevalence, predictors, and consequences of late nephrology referral at a tertiary care center. Early deaths on renal replacement therapy: the need for early nephrological referral. Late referral to maintenance dialysis: detrimental consequences. Late diagnosis of chronic renal failure and mortality on maintenance dialysis. The pattern of referral of patients with end-stage renal disease to the nephrologist— a European survey. UK Renal Registry, The Renal Associaton, The Ninth Annual Report. A population-based study of the incidence and outcomes of diagnosed chronic kidney disease. Unreferred chronic kidney disease: a longitudinal study. Longitudinal follow-up and outcomes among a population with chronic kidney disease in a large managed care organization. Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization. Chronic kidney disease as a global public health problem: approaches and initiatives – a position statement from Kidney Disease Improving Global Outcomes. Chronic kidney diseases in adults: UK guidelines for identification, management and referral. Office for National Statistics population and Vital Statistics, England And Wales. Chronic kidney disease management in the United Kingdom: NEOERICA project results. Prevalence of chronic kidney disease and decreased kidney function in the adult US population: Third National Health and Nutrition Examination Survey. Available from: Centers for Disease Control and Prevention. Prevalence of chronic kidney disease in the United States. JAMA : the Journal of the American Medical Association. The need and demand for renal replacement therapy in ethnic minorities in England. Racial differences in the prevalence of chronic kidney disease among participants in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) Cohort Study.

N atov SN cheap 60 ml rogaine 2 fast delivery, Pereira BJG: H epatitis C infection in patients on dialysis buy 60 ml rogaine 2 fast delivery. LaQ uaglia M P buy rogaine 2 60 ml low cost, Tolkoff-Rubin N E discount 60 ml rogaine 2 with amex, Dienstag JL, et al. Am J Kidney D is 1988, feron therapy on H CV infection of hem odialyzed patients. Kidney Int 1994, tions in renal transplant patients. M ahony JF: Long term results and com plications of transplantation: 110. C virus RN A in organ donors positive for hepatitis C antibody and in the recipients of their organs. Seney FD Jr, Burns DK, Silva FG: Acquired immunodeficiency syndrome Transplantation 1994, 54:832. Vitting KE, Gardenswartz M H , Zabetakis PM , et al. Cockfield SM , Prieksaitis JK: Infection with hepatitis C virus increas- 124. Renal Disease in Patients Infected with Hepatitis and Human Immunodeficiency Virus 7. Clinicopathologic Conference: Fever and acute renal failure in a infections. In Renal and Urologic Aspects of H IV failure due to acyclovir: case report and review of the literature. Valeri A, N eusy AJ: Acute and chronic renal disease in hospitalized 154. Rao TK, Friedman EA: Outcome of severe acute renal failure in patients 131. Rao TK, Friedm an EA: Renal syndrom es in the acquired im m unode- with acquired immunodeficiency syndrome. Am J Kidney Dis 1995, ficiency syndrom e (AIDS): lessons learned from analysis over 5 years. Bourgoignie J: Glom erulosclerosis associated with H IV infection. Bourgoignie JJ: Renal com plications of hum an im m unodeficiency Contem p Issues N ephrol 1996, 29:59–75. Cantor ES, Kim m el PL, Bosch JP: Effect of race on expression of tal glomerulosclerosis in the acquired immunodeficiency syndrome. N acquired im m unodeficiency syndrom e–associated nephropathy. Ann Intern M ed 1984, nephropathy: a detailed m orphologic and com parative study. Clin N ephrol 1984, and safety of cidofovir in patients with hum an im m unodeficiency 21:197–204. M azbar SA, Schoenfeld PY, H um phreys M H : Renal involvem ent in Chem other 1995, 39:882–886. Seidel EA, Koenig S, Polis M A: A dose escalation study to determ ine H ospital. H um phreys M H : H um an im m unodeficiency virus–associated 7:941–945. Rao TKS, Berns JS: Acute renal failure in patients with H IV infections. In m egalovirus retinitis in patients with AIDS: the H PM C peripheral N ephrology, vol 1. Tokyo: Springer-Verlag; cytom egalovirus retinitis trial. Rashed A, Azadeh B, Abu Rom eh SH : Acyclovir-induced acute tubu- occurrence in specific risk groups. N Engl J M ed 1989, sulfadiazine in patients with AIDS. Carbone LG, Bendixen B, Appel GB: Sulfadiazine-associated obstruc- 165. J Am Soc induced crystalluria in AIDS patients with toxoplasm a encephalitis. Cohen AH , N ast CC: H IV-associated nephropathy: a unique com - 143. Becker K, Jablonowski H , H aussinger D: Sulfadiazine-associated bined glom erular, tubular and interstitial lesion. M odern Pathol nephrotoxicity in patients with the acquired im m unodeficiency 1988, 1:87–97. Bourgoignie JJ, Pardo V: The nephropathology in hum an im m uno- 145. Tashim a KT, H orowitz JD, Rosen S: Indinavir nephropathy [letter]. Cohen AH : Renal pathology of H IV-associated nephropathy. Pardo V, Strauss J, Abitbol C: Renal disease in children with H IV 127:119–125. Com iter S, Glasser J, Al-Askari S: Ureteral obstruction in a patient 150:287–292. H um phreys M H : H um an im m unodeficiency virus–associated 149. Shuka RR, Kim m el PL, Jum ar A: M olecular biology of H IV-1 and of the genitourinary tract. J Am Soc Nephrol 1997, peritoneal dialysis and survival of H IV infected patients with end- 8:492A. Casanova S, M azzucco G, Barbiano di Belgiojoso G, et al. Kim m el PL, M ishkin GJ, Um ana W O : Captopril and renal survival in patients with hum an im m unodeficiency virus nephropathy. Korbet SM , Schwartz M M : H um an im m unodeficiency virus infection Kidney D is: 1996, 28:202–208. Kim m el PL, Phillips TM : Im m une-com plex glom erulonephritis associ- 182. W atterson M K, Detwiler RD, Bolin P Jr: Clinical response to pro- ated with H IV infection. Schectman JM , Kimmel PL: Remission of hepatitis B–associated mem- branous glomerulonephritis in human immunodeficiency virus infection.

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These data suggest that selective physio- FIGURE 15-12 logic functions are dim inished after oxidant injury and that a hier- Apoptosis and oncosis are the two generally recognized form s of archy exists in the repair process: m igration or spreading followed cell death generic rogaine 2 60 ml with amex. Apoptosis purchase rogaine 2 60 ml otc, also known as program m ed cell death and by cell proliferation form s a m onolayer and antedates the repair of cell suicide buy rogaine 2 60 ml without prescription, is characterized m orphologically by cell shrinkage purchase 60 ml rogaine 2 visa, cell physiologic functions. In contrast, oncosis, also known as necrosis, necrotic cell death, and cell m urder, is characterized m or- phologically by cell and organelle swelling, plasm a m em brane bleb- bing, cell lysis, and inflam m ation. It has been suggested that cell death characterized by cell swelling and lysis not be called necrosis or necrotic cell death because these term s describe events that occur well after the cell has died and include cell and tissue break- down and cell debris. For m any toxicants, low concentrations cause prim arily apoptosis and oncosis occurs principally at higher concentrations. W hen the prim ary m echanism of action of the Oncosis Oncosis nephrotoxicant is ATP depletion, oncosis m ay be the predom inant cause of cell death with lim ited apoptosis occurring. Apoptosis Apoptosis Toxicant concentration Toxicant concentration Pathophysiology of Nephrotoxic Acute Renal Failure 15. GSH-Hg-GSH Proxim al tubular uptake of inorganic m ercury is thought to be the CYS-Hg-CYS GSH-Hg-GSH result of the transport of m ercuric conjugates (eg, diglutathione γ-GT Urine GLY-CYS-Hg-CYS-GLY? At the lum inal m em brane, GSH -H g-GSH appears Lumen Dipeptidase to be m etabolized by (-glutam yl transferase ((-GT) and a dipepti- CYS-Hg-CYS Na+ dase to form CYS-H g-CYS. The CYS-H g-CYS m ay be taken up by Neutral amino an am ino acid transporter. At the basolateral m em brane, m ercuric –R-Hg-R– + acid transporter conjugates appear to be transported by the organic anion trans- Proximal Na CYS-Hg-CYS tubular cell CYS-Hg-CYS porter. Uptake of m ercuric-protein conjugates by endocytosis Dicarboxylate Organic anion transporter transporter m ay play a m inor role in the uptake of inorganic m ercury trans- port. N ephrotoxicants are generally thought to pro- duce cell injury and death through one of two m echanism s, either Biotransformation alone or in com bination. In som e cases the toxicant m ay have a high affinity for a specific m acrom olecule or class of m acrom ole- High-affinity binding Reactive intermediate Redox cycling cules that results in altered activity (increase or decrease) of these to macromolecules m olecules, resulting in cell injury. Alternatively, the parent nephro- toxicant m ay not be toxic until it is biotransform ed into a reactive Covalent binding Increased reactive interm ediate that binds covalently to m acrom olecules and in turn Altered activity of to macromolecules oxygen species alters their activity, resulting in cell injury. Finally, the toxicant m ay critical macromolecules increase reactive oxygen species in the cells directly, after being bio- transform ed into a reactive interm ediate or through redox cycling. Damage to critical Oxidative damage to The resulting increase in reactive oxygen species results in oxida- macromolecules critical macromolecules tive dam age and cell injury. Cell injury Cell repair Cell death FIGURE 15-16 Plasma RSG Plasma RSG This figure illustrates the renal proximal tubular uptake, biotransfor- Glomerular filtration mation, and toxicity of glutathione and cysteine conjugates and mer- R + SG 1. R-SG R-SG R-SG glutathione conjugate within the renal cell (R-SG). NH +H CCOCO H Basolateral membrane uptake of R-SG (6), R-Cys (7), and a mercap- Na+ 3 3 2 R-SH turic acid (N -acetyl cysteine conjugate; R-NAC)(8). Covalent binding 11) Deacetylation of R-NAC to form R-Cys. Cell injury Plasma of the penultimate nephrotoxic species (R-Cys) by cysteine conjugate R-NAC R-NAC R-NAC R-NAC + 9. Na Basolateral Brush border 13) Binding of the reactive thiol to cellular macromolecules (eg, lipids, membrane membrane proteins) and initiation of cell injury. A, Binding of tetrafluo- roethyl-L-cysteine (TFEC) metabolites in vivo to rat kidney tissue detected immunohisto- chemically. Staining was localized to the S3 segments of the proximal tubule, the segment that undergoes necrosis. C, Isolation and A B fractionation of renal cortical mitochondria from untreated and TFEC treated rats and Representative immunoblot analysis revealed numerous pro- starting Submitochondrial fractions teins that bind to the nephrotoxicant (inner- material A. TFEC (30 mg/kg) inner membrane, matrix-soluble matrix, M (kDa) outer-outer membrane, inter-intermembrane r space). The identity of three of the proteins 228 that bound to the nephrotoxicant: P84, P99 109 mortalin (HSP70-like); P66, HSP 60; and P84 P42, aspartate aminotransferase. The first step, hydrogen HO• Lipid abstraction from the lipid by a radical (eg, hydroxyl), results in the H2O form ation of a lipid radical. Rearrangem ent of the lipid radical Hydrogen abstraction results in conjugated diene form ation. The addition of oxygen •H R results in a lipid peroxyl radical. Additional hydrogen abstraction Lipid radical results in the form ation of a lipid hydroperoxide. The Fenton reac- Diene conjugation tion produces a lipid alkoxyl radical and lipid fragm entation, R resulting in lipid aldehydes and ethane. Alternatively, the lipid per- • oxyl radical can undergo a series of reactions that result in the for- H Lipid radical, conjugated diene m ation of m alondialdehyde. O2 Oxygen addition R R •O–OH Lipid peroxyl radical O O LH Hydrogen abstraction L• R O O Lipid hydroperoxide HOO H Fe(II) Fenton reaction M alondialdehyde • Fe(III) HO R •O H Lipid alkoxyl radical Fragmentation H R • H H H O Lipid aldehyde LH H L• H H Ethane H Pathophysiology of Nephrotoxic Acute Renal Failure 15. In contrast, halocarbon-cysteine conjugate–induced renal proxim al tubular while DEF and DPPD com pletely blocked the lipid peroxidation lipid peroxidation and cell death. The m odel oxidant t-butylhy- caused by DCVC, cell death was only delayed. These results droperoxide (TBH P) and the halocarbon-cysteine conjugate suggest that the iron-m ediated oxidative stress caused by TBH P dichlorovinyl-L-cysteine (DCVC) caused extensive lipid peroxi- is responsible for the observed toxicity, whereas the iron-m ediat- dation after 1 hour of exposure and cell death (lactate dehydro- ed oxidative stress caused by DCVC accelerates cell death. Decreased oxygen delivery secondary to vasoconstriction Inhibition of mitochondrial respiration Increased tubular cell oxygen consumption 15. Citrinin 3 H+ Ochratoxin A Hg2+ CN– 4 Oligomycin 5 + H Pi Pi 6 7 + H M atrix O2 H2O Ochratoxin A 10 Pentachlorobutadienyl–L–cysteine H+ Inner membrane Citrinin FCCP Outer membrane Disruption of ion homeostasis Na+ 100 H2O Na+ 90 80 Na+ + Na+ Na+ ATPase Na ATPase 70 ATP 60 – – Cl– ATP – Cl– 50 QO M embrane – 2 potential Cl– – 40 Cl – K+ – 30 K+ – H2O K+ – 20 10 ATP A K+ B Antimycin A K+ 0 0 5 10 15 20 25 30 Antimycin A Time, min FIGURE 15-22 Early ion m ovem ents after m itochondrial dysfunction. W ithin m inutes of m itochondrial inhibi- FIGURE 15-23 tion (eg, by antim ycin A), ATP levels drop, resulting in inhibition of A graphic of the phenom ena diagram m ed in Figure 15-22. B, Consequently, N a+ influx, K+ efflux, m em - brane depolarization, and a lim ited degree of cell swelling occur. FIGURE 15-24 Na+ + The late ion m ovem ents after m itochondrial dysfunction that leads Na - to cell death/lysis. A, Cl influx occurs as a distinct step subsequent ATPase + + - + Na+ to N a influx and K efflux. B, Following Cl influx, additional Na ATPase N a+ and water influx occur resulting in term inal cell swelling. ATP Cl Cl Cl– Cl– K+ + K H2O Antimycin A K+ Antimycin A K+ A B Pathophysiology of Nephrotoxic Acute Renal Failure 15. FIGURE 15-27 Biochem ical characteristics of calpain. Proposed pathways of calpain activation and translocation. Both calpain subunits m ay undergo calcium (Ca2+)-m ediated autolysis within the cytosol and hydrolyze cytoso- lic substrates.

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